Q: "One of my friends said they heard you discuss the difference between
albinos and black-eyed whites at [Ferrets 2000]. They said you indicated
albinism was proof of domestication....How?"

Ah! A person who understands the difference between a philosophical
question, why, and a mechanistic question, how. Can you please explain
the difference to the more rabid creationists?

Albinism in ferrets is due to a recessive allele on a single chromosome
(actually, a pair of recessive alleles on a pair of matched
chromosomes). Because the allele is recessive, it requires the ferret to
have two copies for the trait to be expressed. This is a truly recessive
allele in ferrets, which means without two copies, there can be no
expression of the trait in any form. In other words, this trait does not
blend, nor it does it partially express; you either have two copies and
are an albino, or you have zero or a single copy and you are notthere
are no in-betweens. In non-domesticated species, albinism is extremely
rare because the chances of getting two copies of the allele is so
remote. In the wild, it is more commonly seen in species where the
breeding population is small, but even then, it is quite rare. Even in
those instances where albinism occurs in the wild, it never persists as
a trait, being bred out of the species relatively rapidly, as will be
explained below.

In ferrets, albinism is persistent; that is, the allele has reached a
stable frequency of expression within the population and would not breed
out during random mating (assuming no change in selective pressures). In
other words, if you randomly selected 100 females out of a randomly
mixed breeding pool of ferrets, and mated them to 100 male ferrets, also
randomly selected from a randomly mixed breeding pool, then the
offspring would express albinism at approximately the same frequency as
in the parents, as would succeeding generations. Ferrets are not the
only animal which has persistent albinism; it also occurs in rabbits,
mice, rats, chickens, doves, and other human-selected (or domesticated)
animals. Thus, persistent albinism is evidence of domestication, and is
only found when humans selective breed for the trait. Indeed, it can
only occur in a state of domestication; a recessive trait, albinism
cannot persist in wild populations, especially those subjected to both
predation and starvation selective pressures (like what would be
expected with such a predator as the ferret). Since historic references
can document the condition in ferrets for most of the last 1000 years,
that alone is pretty good evidence ferrets are domesticated (most
reports from earlier ages discuss ferrets, but do not describe their
outward or physical appearance). In other words, long term, persistent
albinism is absolute evidence that ferrets have been bred, housed and
cared for by humans, and that hybridization to wild species has been
minimal for at least since the first report of the trait. Persistent
albinism is simply not a trait of a non-domesticated (wild) population.

Such a long span of time, coupled with ancient husbandry methods, has
"bred out" many of the problems associated with the inbreeding necessary
to establish albinism as a persistent trait (let no imperfect animal go
unculled; culling was thought to maintain the perfection God required in
the animal). This includes the worst expressions of some of the
characteristic aspects of albinism (nothing major, just a simple skewing
of the bell curve towards the "we can live with it" side). For
centuries, albino ferrets were preferred throughout Europe for rabbiting
because the white coats were thought easier to spot exiting burrows.
Poachers also preferred albinos because they could be seen easier in the
dark. Many 300+ year old reports on ferrets considered only the albino
coloration to be a true ferret, calling the "polecat color" either
semi-domesticated or "wild but tamed". It doesn't take a lot of
generations, if carefully culled, for the really bad side effects of
inbreeding to be removed from a breeding population. Nor does it take
much longer to skew the normal distribution of albinistic characters
towards the beneficial side; not actually making albinism beneficial,
but rather reducing the negative impact so it is easier on the ferret.
So, even though albinism causes some problems in ferrets, generally
speaking, they can easily live with them. The result is an animal with
what is essentially a birth defect, but who doesn't exhibitat a
population levelthe great numbers of really bad side effects which
would be expected. The reason I use the term "birth defect" is because
the albino "gene" is essentially a mutated allele of a normal gene.
Strictly speaking, there is no gene that codes for albinism. Rather,
there is a mutated allele which codes for pigmentation, but which
doesn't work, and when you have two of them and no way to make pigment,
then you are an albino.

This is a completely different thing than the partial depigmentation
that can be caused by human selection for tameness. While on the
surface, "albinism" and "depigmentation" appear synonymous, they are not
strictly so. An albino ferret cannot make pigments, but may have genetic
code for any number of coat colors which could be expressed in a
heterozygous offspring. A depigmented ferret is just that, a ferret
which can code for pigment, but for some reason, pigments are not being
made or deposited. An animal can become depigmented for metabolic
reasons (seasonal white fur, gray hair), or because of a disruption in
the timing of distribution of pigmented cells during early embryonic
development (blazes, white faces and bibs, white feet). For example,
fox, snowshoe hares and ermine are seasonally depigmented, as are
ferrets to a minor degree. Polar bears have evolved white fur, but they
are not depigmented. Those animals (almost exclusively domesticated, but
including humans) having blazes, stripes, piebald coloration, or white
foreheads and bibs are developmentally depigmented. Most depigmentation
occurs because of a metabolic disruption of normal pigmentation, and is
an evolved trait which produces seasonal coat coloration changes. This
is typically tied to photoperiod cycles and is regulated by hormones.
But in domesticated animals, something else is happening; depigmentation
occurs because the cells which produce pigments are prevented from
reaching their final destinations, leaving specific areas void of
pigmented cells. See the difference? In albinos, pigmented cells are
normally distributed, but they lack the ability to produce pigments. In
developmentally depigmented animals, pigments are produced normally, but
some areas lack pigmented cells. In domesticated animals, developmental
depigmentation is a result of breeding for tameness.

There is a fairly well documented hypothesis called the "Star Gene"
which ties the behavioral changes caused by domestication to piebalding,
neotony, and a host of other morphological changes, mostly of a visual
and auditory nature (The Star Gene is named after the star of white
commonly seen on the foreheads of animals possessing the trait). In an
extremely short and simple explanation, breeding for tameness (reducing
fight/flight distance to zero) results in changes in the timing of brain
development, interfering with the migration of pigmented cells during
early embryonic development. This results in human friendly animals, but
it also results in stars, blazes or light colored stripes on the head
and forehead, white faces, chest blazes, white feet or knees,
generalized piebalding; that sort of thing. It can also result in some
significant hearing and vision problems, far beyond those caused by
albinism. Interestingly enough, a ferret with a strong expression of the
"Star Gene" resulting in deafness and visual problems, may also be an
albino. Because you don't see the piebalding clues, some people can
erroneously attribute the bad side effects to problems caused by
albinism, when in reality it is due to piebalding (Waardenburg's
Syndrome is closely associated with piebalding, the outward expression
of the Star Gene).

Current domestication theory more-or-less accepts the Star Gene
hypothesis as valid because it is the simplest explanation for nearly
identical changes in different species. For example, most domesticated
animals have members in the population which exhibit piebalding
(brown/black coloration), shortened faces with exaggerated foreheads
(cranial neotony), persistence of juvenile behaviors (behavioral
neotony), and changes in the reproductive timing cycles (increased
breeding) (Note: piebalding is an irregular brown/black and white
colorationthat stupid computer "cow" box is piebald). All these
traitsand many morecan be traced either to changes in brain
development due to domestication, OR to changes in genes closely linked
to the Star Gene. This is still considered an hypothesis because the
Star Gene has yet to be found and the mechanisms of the Star Gene Effect
are still mostly unknown. It may be a single gene, or more likely, a
series of genes that are linked together in some way (either because
they are adjacent to each other on the chromosome or because they are
developmentally linked), so that changes in the keystone genethe Star
Generesults in changes to the linked genes. Most of these changes are
thought to be disruptions in embryonic timing, but some are due to
environmental influences (metabolic and biochemical changes).

One of the tests of the Star Gene hypothesis is that the results of
breeding should be somewhat unpredictable. Because the Star Gene changes
the developmental timing in the embryo, extremely slight changes due to
environmental influences can result in major differences in expression.
In other words, just a few minutes in timing one way or another can
result in the extension of a blaze into a stripe, or the difference
between diminished hearing and deafness. This makes breeding for these
traits somewhat unpredictable; you may know you will get a blaze of some
type, but you cannot predict the degree of expression for trait because
it is so environmentally sensitive. (Note: we will never know exactly
HOW much hearing loss is present in ferrets because we only test for the
presence or absence of hearing, not for the degree of diminished
hearing. Thus it is probable hearing disorders are far more common than
generally perceived).

In ferrets, pandas, white faces, bibs, stripes, white mitts, white
knees, and blazes are all thought to be expressions of the Star Gene,
which is why ferrets with those markings are so subject to visual and
auditory problems (and other problems common to Waardenburg's Syndrome).
Silvers and dark eyed whites are not due to albinism, nor because of the
expression of the Star Gene, but rather because of manipulation of the
various genes (and their alleles) which code for color (the genes for
color are thought to exist in at least three different locations, on at
least two different chromosomes). In other words, a dark eyed white
ferret is white for the same reasons polar bears are white; because
their color genes code for it, NOT because they are albino or have a
strong expression of the Star Gene, although both are possible. The way
you can discern the difference between depigmentation due to breeding
for tameness from naturally occurring instances is by coexistent
changes, including cranial differences and behavioral neotony, which do
not exist in wild populations. Star Gene mediated depigmentation is only
present in domesticated animals because it is a result of breeding for tameness.

So, since we know persistent albinism and depigmentation caused by the
expression of the Star Gene is only found in domesticated animals, and
since we also know albinism in ferrets is at least 1000 years old and
that Star Gene depigmentation is common, then we know the ferret has had
a long period of domestication, with breeding for tameness common and
under human control. In other words, the fact that you can commonly see
albino ferrets, or ferrets with blazes, stripes, or panda markings, we
knowbeyond a shadow of a doubtthat ferrets are quite domesticated. We
also know the genetics of ferret coloration is quite complicated, with
three major elements to be complicating factors in predicting the
results of breeding (genes controlling normal pigmentation, the
migration of pigmented cells, and coat coloration).